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Am J Physiol Gastrointest Liver Physiol (April 15, 2004). doi:10.1152/ajpgi.00314.2003
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Submitted on July 23, 2003
Accepted on April 2, 2004

Lipopolysaccharides induced increases in Fas-ligand expression by Kupffer cells via mechanisms dependent on reactive oxygen species

Keiichiro Uchikura1, Tatehiko Wada1, Sumito Hoshino1, Yuichi Nagakawa1, Takashi Aiko2, Gregory B. Bulkley1, Andrew S. Klein1, and Zhaoli Sun1*

1 Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
2 First Department of Surgery, Faculty of Medicine, Kagoshima University, Kagoshima, Kagoshima, Japan

* To whom correspondence should be addressed. E-mail: zlsun{at}jhmi.edu.

Fas-Fas ligand (FasL) dependent pathways exert a suppressive effect upon inflammatory responses in immune-privileged organs. FasL expression in hepatic Kupffer cells (KC) has been implicated in hepatic immunoregulation. In this study, modulation of FasL expression of KC by endogenous gut-derived bacterial lipopolysaccharides (LPS), and the role of reactive oxygen species (ROS), as potential mediators of FasL expression in KC were investigated. LPS stimulation of KC resulted in upstream ROS generation and subsequently increased FasL expression, and consequent Jurkat cell (Fas+) apoptosis. The NADPH oxidase and the xanthine oxidase enzymatic pathways both appear to be major sources of this upstream ROS generation. Increased FasL expression was blocked by antioxidants and by blocking ROS generation enzymatically. The exogenous administration of H2O2 stimulated both KC FasL expression and subsequent Jurkat cell apoptosis. Intracellular endogenous ROS generation may, therefore, represent an important signal transduction pathway for FasL expression in KC.




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